Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The amino acid content of plasma and erythrocytes in patients with severe renal failure (serum creatinine less than 8 mg/100 ml) treated with selective low-protein diets, in patients on regular hemodialysis, and in a control group of healthy subjects were studied. Most amino acids in erythrocytes of the patients showed the same changes as in plasma with the exception of histidine, serine, and alanine. In spite of low histidine plasma levels, the erythrocytes level is increased as compared with healthy controls. In uremic patients the plasma serine was constantly reduced whereas the serine content of the erythrocytes did not differ from healthy controls. Alanine concentrations in the erythrocytes of uremic patients were increased in spite of normal alanine plasma levels. This finding may be due to the increased glycolytic ratio of red cells from uremic subjects delivering more pyruvate for transmination to alanine. In the control group the cysteine content of erythrocytes was decreased with a gradient between plasma and erythrocytes of 3.5:1. The same gradient could be observed in uremic patients in spite of the elevation in their plasma cysteine levels by a factor of 2.7 compared with controls. The low cysteine levels in erythrocytes may be due to loss of cysteine for glutathione synthesis in red cells. High glutathione levels in the erythrocytes of uremic patients support this hypothesis.
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PMID:Amino acid content of erythrocytes in uremia. 70 55

We have compared the disposition of oral paracetamol (1.0 g t.d.s. for 10 days) in 6 healthy volunteers and 6 conservatively-managed patients with chronic renal failure (mean plasma creatinine 451 mumol.l-1). Blood was sampled daily for 10 days before the morning dose of paracetamol. Each day the pretreatment plasma concentrations of paracetamol were higher in the renal failure patients than in the volunteers, with mean values over the 10 days of 3.1 and 1.1 mg.l-1 respectively. The mean daily plasma concentrations of the sulphate and glucuronide conjugates of paracetamol were markedly higher in the renal failure group and apparent steady-state concentrations of about 25 and 85 mg.l-1 were reached on the 2nd and 6th days respectively. The mean steady-state plasma concentrations of the glucuronide conjugate on the 7th to 10th days of treatment were positively correlated with the plasma creatinine concentration (r = 0.97), but this relationship did not hold for the sulphate conjugate. Cysteine and mercapturate conjugates could only be detected in one patient. Predictions of steady-state concentrations based on previous studies with single doses of paracetamol in renal failure patients were remarkably accurate for the glucuronide but not for the sulphate conjugate. These results are consistent with some extra-renal elimination of retained paracetamol conjugates in patients with chronic renal failure, with limited regeneration of the parent compound. The sulphate metabolite did not accumulate as predicted, possibly because of depletion of inorganic sulphate.
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PMID:The disposition of paracetamol and the accumulation of its glucuronide and sulphate conjugates during multiple dosing in patients with chronic renal failure. 178 75

Essential amino acids, found in abundance in high-quality dietary protein, are required daily by hospitalized patients and healthy persons to maintain the dynamic process of protein metabolism. One method for assessing dietary protein quality is by determining a diet's chemical score, ie, the ratio of a gram of the limiting amino acid in a test diet to the same amount of the corresponding amino acid in a reference diet (eg, whole-egg protein) multiplied by 100. This investigation used the chemical score to evaluate the protein quality of 9 parenteral and 17 enteral diets commonly used to feed hospitalized patients. Standard parenteral and enteral products (ie, formulas that had not been designed for patients with a specific disease state) had chemical scores that ranged from 46% to 70%. Limiting amino acids were either methionine (plus cysteine) or phenylalanine (plus tyrosine). Products designed for patients with renal failure had the highest scores, which ranged from 85% to 145%. Products that were enriched with branched-chain amino acids for trauma patients had scores that ranged from 38% to 73%. The only product available for patients with pulmonary compromise had a score of 50%. The lowest scores, which ranged from 5% to 13%, were found in products for patients with hepatic failure. All products, except those with chemical scores below 13%, may be fed in relatively small amounts of protein (7 to 33 g) to satisfy the minimum daily requirements of essential amino acids, although such levels would not meet minimal daily nitrogen requirements. We recommend that dietitians use the chemical score to assess the protein quality of parenteral and enteral diets.
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PMID:A chemical score to evaluate the protein quality of commercial parenteral and enteral formulas: emphasis on formulas for patients with liver failure. 190 41

Plasma homocyst(e)ine (the sum of free and bound homocysteine, homocystine, and the mixed disulfide homocysteine-cysteine, expressed as homocysteine) levels were determined by high performance liquid chromatography in 214 patients with symptomatic (claudication, rest pain, gangrene, amputation) lower extremity arterial occlusive disease and/or symptomatic (stroke, cerebral transient ischemic attacks) cerebral vascular disease and in 103 control persons. Mean plasma homocyst(e)ine was significantly higher in patients than in controls (14.37 +/- 6.89 nmol/ml vs 10.10 +/- 2.16, p less than 0.05). Thirty-nine percent of patients (83 of 214) had plasma homocyst(e)ine values greater than control mean + 2 standard deviations. Plasma homocyst(e)ine values were contrasted to age, male sex, diabetes, hypertension, smoking, renal failure, and plasma cholesterol. No difference was found in the incidence and/or level of any of these risk factors when patients with normal plasma homocyst(e)ine were compared to those with elevated plasma homocyst(e)ine, both by univariate and multivariate analysis. Patients with elevated plasma homocyst(e)ine were more likely to demonstrate clinical progression of lower extremity disease and of coronary artery disease, but not of cerebral vascular disease than were patients with normal plasma homocyst(e)ine, and the rate of progression was more rapid (p = 0.002). Progression of lower extremity disease as assessed in the vascular laboratory was also more common in patients with elevated plasma homocyst(e)ine (p = 0.01). We conclude that elevated plasma homocyst(e)ine is an independent risk factor for symptomatic lower extremity disease or cerebral vascular disease or both. Symptomatic patients with lower extremity disease and with elevated plasma homocyst(e)ine also appear to have more rapid progression of disease.
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PMID:The association of elevated plasma homocyst(e)ine with progression of symptomatic peripheral arterial disease. 198 84

The disposition of paracetamol following an oral dose of 1.0 g was compared in 10 healthy volunteers, 7 patients with moderate chronic renal failure and 6 patients with end stage renal failure on maintenance haemodialysis. Paracetamol absorption was normal in the patients with renal failure. The mean plasma half-life of paracetamol from 2 to 8 h was similar in the 3 groups (2.1 to 2.3 h) but from 8 to 24 h it disappeared much more slowly in the renal failure patients (half-life 11.7 compared with 4.9 h in the healthy volunteers). Plasma concentrations of paracetamol glucuronide and sulphate conjugates were greatly increased in the patients with moderate renal failure and the mean plasma half-lives were 30.5 and 21.8 h respectively compared with about 3 h in the healthy volunteers. Plasma concentrations of these metabolites were even higher in the dialysis patients and there was no significant fall over 24 h. The cysteine and mercapturic acid conjugates of paracetamol could only be measured in plasma in the patients with renal failure and concentrations were very low. The fractional urinary recovery of paracetamol and its glucuronide, sulphate, cysteine and mercapturic acid conjugates was similar in healthy volunteers and patients with moderate renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Paracetamol disposition and metabolite kinetics in patients with chronic renal failure. 274 70

Homocysteine is a branch-point metabolite, the biological fate of which is linked to vitamin B12, reduced folates and vitamin B6. Various inborn defects in homocysteine metabolism, among which cystathionine beta-synthase deficiency is most common, lead to the clinical condition homocystinuria. A central feature of this clinical state is premature arteriosclerosis. These patients benefit from agents serving as cofactors in homocysteine metabolism which both reduce the homocysteine levels in plasma and the incidence of vascular episodes. Experimental data point to homocysteine as an arteriosclerotic agent. Homocysteine in human plasma exists mainly as mixed disulfides with albumin (70 per cent) and cysteine. New methods determine total plasma homocysteine which includes all these species. Normal values for plasma homocysteine are lower in premenopausal women than in men and postmenopausal women. Impaired homocysteine metabolism seems to exist in 15-30 per cent of patients with premature cardiovascular disease. Moderate homocysteinemia is as a risk factor for cardiovascular disease, independent of conventional risk factors. Apart from homocystinuria, vitamin B12 deficiency causes the most extreme elevations of plasma homocysteine, and it has been established that plasma homocysteine is a more responsive parameter to impaired vitamin B12 function than serum cobalamin. Massive increase in plasma homocysteine level is also observed in folate deficiency, whereas renal failure, some malignant states and psoriasis cause a moderate homocysteinemia. High doses of folic acid reduce plasma homocysteine, and this innocuous mean should be considered as an intervention in patients with increased plasma level. Drugs like methotrexate, some anticonvulsants and 6-azauridine triacetate induce moderate elevation of plasma homocysteine, whereas a reduction is observed after penicillamine administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Plasma homocysteine, a risk factor for premature vascular disease. Plasma levels in healthy persons; during pathologic conditions and drug therapy]. 281 54

Serum levels of proteins reactive in radioimmunoassay with an antiserum prepared in rabbits against purified human spleen neutral cysteine proteinase inhibitor (NCPI) was determined in 70 healthy controls and from 80 patients suffering from suspected or proven kidney failure. The values varied from less than 0.2 mg/l in normal sera to levels over 2 mg/l in some patient sera. Serum level of NCPI was found to roughly correlate with serum creatinine values. However, there were sera with high NCPI levels which did not have increased serum creatinine values. In sera with high NCPI levels subjected to double radial immunodiffusion two precipitin lines, one completely and the other partially identical to NCPI were registered. After fractionating of serum proteins with gel chromatography on Sephadex G 100, two protein peaks of immunological similarity to purified NCPI were found: one low molecular weight (MW around 12,000) and one high molecular weight (MW around 100,000). The low molecular weight NCPI-like material appeared to inhibit human cathepsin B and papain and is thus free serum NCPI. alpha-Cysteine proteinase inhibitor did not increase with serum creatinine as did NCPI.
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PMID:Serum cysteine proteinase inhibitors with special reference to kidney failure. 391 39

1. Plasma sulphur-containing amino acids were measured in 19 patients with renal failure on chronic haemodialysis and in 22 normal subjects, to determine the rate of accumulation of these amino acids in chronic azotaemia. 2. Cysteine--homocysteine mixed disulphide was significantly increased in patients before dialysis and homocysteine was detected in low concentration in 10 patients. Cystine and taurine were also increased. Changes in other neutral and acidic amino acids were similar to those reported in chronic renal insufficiency. 3. In 3--4 h of dialysis serum creatinine was decreased by a mean of 55%, cysteine--homocysteine by 41% and cystine by 58.5% (P less than 0.001 for each). Methionine concentrations were normal throughout. 4. We conclude that sulphur-containing amino acids, except methionine, accumulate in chronic renal failure as rapidly as creatinine.
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PMID:Accumulation of sulphur-containing amino acids including cysteine-homocysteine in patients on maintenance haemodialysis. 738 71

The levels of different fractions of homocysteine, cysteine and cysteinylglycine were investigated in 17 patients on chronic hemodialysis, 9 patients with reduced renal function and 4 patients with nephrotic syndrome and compared with 14 healthy subjects. Total plasma homocysteine, cysteine and cysteinylglycine were increased in the patients with reduced renal function and in those on chronic hemodialysis. The free (non-protein-bound) forms of plasma homocysteine and cysteine were significantly increased in all groups of patients. The reduced forms of plasma homocysteine and cysteine were, however, not increased in any of the patient groups; on the contrary, reduced plasma homocysteine was significantly decreased in the group of patients with reduced renal function. These findings indicate that the plasma levels of reduced forms of the thiol compounds are relatively normal and do not merely mirror the elevation of the disulfide forms. The possible relation between homocysteine and increased atherogenesis in patients with renal failure is discussed.
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PMID:Reduced, free and total fractions of homocysteine and other thiol compounds in plasma from patients with renal failure. 761 18

Despite longstanding interest by nephrologists and physiologists, the molecular identities of membrane water channels remained elusive until recognition of CHIP, a 28-kDa channel-forming integral membrane protein from human red blood cells originally referred to as "CHIP28." CHIP functions as an osmotically driven, water-selective pore; 1) expression of CHIP conferred Xenopus oocytes with markedly increased osmotic water permeability but did not allow transmembrane passage of ions or other small molecules; 2) reconstitution of highly purified CHIP into proteoliposomes permitted determination of the unit water permeability, i.e., 3.9 x 10(9) water molecules.channel subunit-1 x s-1. Although CHIP exists as a homotetramer in the native red blood cell membrane, site-directed mutagenesis studies suggested that each subunit contains an individually functional pore that may be reversibly occluded by mercurial inhibitors reacting with cysteine-189. CHIP is a major component of both apical and basolateral membranes of water-permeable segments of the nephron, where it facilitates transcellular water flow during reabsorption of glomerular filtrate. CHIP is also abundant in certain other absorptive or secretory epithelia, including choroid plexus, ciliary body of the eye, hepatobiliary ductules, gall bladder, and capillary endothelia. Distinct patterns of CHIP expression occur at these sites during fetal development and maturity. Similar proteins from other mammalian tissues and plants were later shown to transport water, and the group is now referred to as the "aquaporins." Recognition of CHIP has provided molecular insight into the biological phenomenon of osmotic water movement, and it is hoped that pharmacological modulation of CHIP function may provide novel treatments of renal failure and other clinical problems.
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PMID:Aquaporin CHIP: the archetypal molecular water channel. 769 81


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